Ni Interdiffusion Coefficient and Activation Energy in Cu6Sn5

Ni diffusion in Cu6Sn5 intermetallic compound was investigated. First, we successfully fabricated preferred-orientation Cu6Sn5 crystal by liquid-phase electroepitaxy (LPEE). Then, Ni/Cu6Sn5 diffusion couples were produced by sputtering from a Ni thin film onto the Cu6Sn5 crystal. Ni/Cu6Sn5 diffusion couples were annealed at different temperatures of 120A degrees C, 160A degrees C, 200A degrees C, 255A degrees C, 290A degrees C, and 320A degrees C for 2 h in a vacuum. The Ni atomic profile across the Ni/Cu6Sn5 interface was obtained by electron spectroscopy for chemical analysis (ESCA). From the Ni atomic profiles, the Matano method was used to evaluate the Ni interdiffusion coefficients ((D) over tilde (Ni)) in the Cu6Sn5 crystal obtained with different annealing temperatures, which then yields the activation energy for Ni diffusion in the Cu6Sn5 crystal at a particular Ni content. We found that, as Ni diffuses in the ternary Cu6-x Ni (x) Sn-5 compound phase, the activation energy of Ni interdiffusion decreases with the Ni content

Dewetting Retardation on Ag/Cu Coated Light Emitting Diode Lead Frames During the Solder Immersion Process

The process of SnPb immersion in Ag/Cu coated light emitting diode lead frames (LED LFs) (alloy 42) was investigated. SnPb solder was found to cause dewetting of the LF substrate after 6 s of immersion. We believed that the dewetting of the SnPb solder could be attributed to spalling of the interfacial compound grains. The addition of a small amount of Ni to the molten SnPb solder (0.1 wt.%) retarded that spalling and helped to prevent dewetting. The mechanisms for spalling retardation by the addition of Ni additives are as follows: (1) the Ni additives slow down the reaction rate between the molten SnPb solder and the Ag/Cu plating layer; (2) the Ni additives participate in interfacial reactions to form (Cu,Ni)(6)Sn(5) ternary compounds, which are more stable than binary compounds and have a slower ripening process

Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population

Lung adenocarcinoma is the most common type of lung cancer. Known risk variants explain only a small fraction of lung adenocarcinoma heritability. Here, we conducted a two-stage genome-wide association study of lung adenocarcinoma of East Asian ancestry (21,658 cases and 150,676 controls; 54.5% never-smokers) and identified 12 novel susceptibility variants, bringing the total number to 28 at 25 independent loci. Transcriptome-wide association analyses together with colocalization studies using a Taiwanese lung expression quantitative trait loci dataset (n = 115) identified novel candidate genes, including FADS1 at 11q12 and ELF5 at 11p13. In a multi-ancestry meta-analysis of East Asian and European studies, four loci were identified at 2p11, 4q32, 16q23, and 18q12. At the same time, most of our findings in East Asian populations showed no evidence of association in European populations. In our studies drawn from East Asian populations, a polygenic risk score based on the 25 loci had a stronger association in never-smokers vs. individuals with a history of smoking (Pinteraction = 0.0058). These findings provide new insights into the etiology of lung adenocarcinoma in individuals from East Asian populations, which could be important in developing translational applications

Transcription of Xanthomonas campestris prt1 gene encoding protease 1 increases during stationary phase and requires global transcription factor Clp (vol 295, pg 43, 2002)

Xanthomonas campestris pv. campestris produces three proteases, Prt1, Prt2, and Prt3, the first two of which are involved in pathogenicity. In this study, nucleotide A 84 nt upstream of the prt1 start codon, which is 8 nt downstream of the -10 sequence, was determined as the transcription start site by the 5' RACE (rapid amplification of cDNA ends) method. Using Pprt1-lacZ transcriptional fusion constructs for assays, several interesting characteristics of prt1 promoter were revealed. The expression is inducible by LB medium or casein proteins and involves the global transcription factor Clp (cyclic AMP receptor protein-like protein). The region containing by -392 to -80 relative to the prt1 translation initiation codon is required for maximal expression, in which by -392 to -207 responds to the Clp-mediated regulation and the induction. In presence of inducers and the clp wild-type background, the levels of expression continue to increase following cell growth until 30h after the cultures entering stationary phase. Since prt1 promoter shows no response to stressful conditions and neither growth nor cell viability is affected by prt1 mutation, Prt1 appears to be a secondary metabolite of X. campestris pv. campestris. (C) 2002 Elsevier Science (USA). All rights reserved

Predator-prey model with disease infection in both populations

A predator-prey model with disease infection in both populations is proposed to account for the possibility of a contagious disease crossing species barrier from prey to predator. We obtain several threshold parameters from local analysis of various equilibria of the proposed system as well as coupled conditions on these threshold parameters which determine the stability of these equilibria. One of the coupled conditions, in the form of an ecological threshold number for the predator-prey ecosystem, always determines the coexistence of predators and prey. The other condition, in the form of a disease basic reproduction number, dictates whether the disease will become endemic in the ecosystem. Under one combination of these coupled conditions, a highly infectious disease could drive the predators to extinction when predators and prey would have coexisted without the disease. For another combination of the conditions, the predation of the more vulnerable infected prey could cause the disease to be eradicated in the ecosystem, in some case even approaching a disease-free periodic solution, when the disease would have otherwise remained endemic in the prey population in the absence of predation. This indicates that the presence of disease in both predators and prey could either promote or impair coexistence, and its precise impact needs to be explored specifically in each particular situation. By considering disease infection in both populations, our model also yields more complex dynamics, allowing for the possibility of bistability and periodic oscillation, in either disease-free or endemic states, in the ecosystem for which the conditions are obtained analytically and with the help of numerical simulations

Clp upregulates transcription of engA gene encoding a virulence factor in Xanthomonas campestris by direct binding to the upstream tandem Clp sites

In Xanthomonas campestris, the causative agent of black rot in crucifers, the endoglucanase level is greatly decreased in the mutant deficient in Clip, a homologue of cyclic AMP receptor protein (CRP). It is established that Clp has the same DNA binding specificity as CRP at positions 5, 6, and 7 (GTG motif) of the DNA half site. In this study, the engA transcription initiation site was determined by the 5' RACE method, and two consensus Clp-binding sites, site I and site II centered at -69.5 and -42.5, respectively, were located. Transcriptional fusion assays indicated that Clp greatly activates engA transcription. Site-directed mutagenesis indicated that position 5 of GTG motif in site II is essential for both DNA-protein complex formation in electrophoretic mobility shift assays and engA transcription in vivo. In addition, mutation at position 5 of site I drastically reduces the promoter activity, indicating that binding of Clp to site I exerts a synergistic effect on the transcription activation by site II. engA appears to be the first X. campestris gene known to be activated by Clp via a direct binding to the promoter. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V.. All rights reserved